Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?
Identifieur interne : 000441 ( Istex/Corpus ); précédent : 000440; suivant : 000442Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?
Auteurs : A. Buske-Kirschbaum ; S. Jobst ; D. H. HellhammerSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 1998-05.
Abstract
Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.
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DOI: 10.1111/j.1749-6632.1998.tb09613.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title><author><name sortKey="Buske Irschbaum, A" sort="Buske Irschbaum, A" uniqKey="Buske Irschbaum A" first="A." last="Buske-Kirschbaum">A. Buske-Kirschbaum</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Jobst, S" sort="Jobst, S" uniqKey="Jobst S" first="S." last="Jobst">S. Jobst</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D. H." last="Hellhammer">D. H. Hellhammer</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: hellhamm@pcmail.uni‐trier.de</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8F433D0008258B11E0B66804EDBBB8DC8A64220B</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1111/j.1749-6632.1998.tb09613.x</idno><idno type="url">https://api.istex.fr/document/8F433D0008258B11E0B66804EDBBB8DC8A64220B/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000441</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000441</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title><author><name sortKey="Buske Irschbaum, A" sort="Buske Irschbaum, A" uniqKey="Buske Irschbaum A" first="A." last="Buske-Kirschbaum">A. Buske-Kirschbaum</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Jobst, S" sort="Jobst, S" uniqKey="Jobst S" first="S." last="Jobst">S. Jobst</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D. H." last="Hellhammer">D. H. Hellhammer</name><affiliation><mods:affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: hellhamm@pcmail.uni‐trier.de</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-05">1998-05</date><biblScope unit="volume">840</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="747">747</biblScope><biblScope unit="page" to="754">754</biblScope></imprint><idno type="ISSN">0077-8923</idno></series><idno type="istex">8F433D0008258B11E0B66804EDBBB8DC8A64220B</idno><idno type="DOI">10.1111/j.1749-6632.1998.tb09613.x</idno><idno type="ArticleID">NYAS747</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>A. BUSKE‐KIRSCHBAUM</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</json:string></affiliations></json:item><json:item><name>S. JOBST</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</json:string></affiliations></json:item><json:item><name>D. H. HELLHAMMER</name><affiliations><json:string>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</json:string><json:string>E-mail: hellhamm@pcmail.uni‐trier.de</json:string></affiliations></json:item></author><articleId><json:string>NYAS747</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.</abstract><qualityIndicators><score>1.86</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 842 pts (A4)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1092</abstractCharCount><pdfWordCount>12</pdfWordCount><pdfCharCount>113</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>154</abstractWordCount></qualityIndicators><title>Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title><refBibs><json:item><host><author></author><title>Ruzicka, T., J. Ring & B. Przybilla, Eds. 1992. Handbook of Atopic Eczema. Springer Verlag. Berlin.</title></host></json:item><json:item><host><author></author><title>Rajka, G. 1993. Essential aspects of atopic eczema. Springer Verlag. Berlin.</title></host></json:item><json:item><author><json:item><name>J. Ring</name></json:item></author><host><volume>101</volume><pages><last>307</last><first>305</first></pages><author></author><title>Int. Arch. Allergy Immunol.</title></host><title>Atopic diseases and mediators</title></json:item><json:item><author><json:item><name>D. Y. M. Leung</name></json:item></author><host><volume>12</volume><pages><last>346</last><first>339</first></pages><author></author><title>Allergy Proc.</title></host><title>Immune mechanisms in atopic dermatitis and relevance to treatment</title></json:item><json:item><author><json:item><name>G. Marone</name></json:item></author><host><volume>77</volume><pages><last>106</last><first>103</first></pages><author></author><title>Int. Arch. Allergy Appl. Immunol.</title></host><title>Studies on human basophil releasability</title></json:item><json:item><author><json:item><name>A. Kapp</name></json:item></author><host><volume>25</volume><pages><last>219</last><first>210</first></pages><author></author><title>Clin. Exp. Allergy</title></host><title>Atopic dermatitis‐the skin manifestation of atopy</title></json:item><json:item><author><json:item><name>G. C. Mudde</name></json:item></author><host><volume>69</volume><pages><last>341</last><first>335</first></pages><author></author><title>Immunology</title></host><title>Allergen presentation by epidermal Langerhans' cells from patients with atopic dermatitis is mediated by IgE</title></json:item><json:item><author><json:item><name>E. A. Wierenga</name></json:item></author><host><volume>147</volume><pages><last>2949</last><first>2942</first></pages><author></author><title>J. Immunol.</title></host><title>Human atopen‐specific types 1 and 2 T helper cell clones</title></json:item><json:item><host><author></author><title>Kapp, A. 1992. Cytokines in atopic eczema. In Handbook of Atopic Eczema. T. Ruzicka, J. Ring & B. Rpzybilla, Eds. Vol. 1: 256‐262. Springer Verlag. Berlin.</title></host></json:item><json:item><author><json:item><name>W. Czech</name></json:item></author><host><volume>126</volume><pages><last>355</last><first>351</first></pages><author></author><title>Br. J. Dermatol.</title></host><title>Serum eosinophil cationic protein (ECP) is a sensitive measure for disease activity in atopic dermatitis</title></json:item><json:item><author><json:item><name>J. Marx</name></json:item></author><host><volume>270</volume><pages><last>233</last><first>232</first></pages><author></author><title>Science</title></host><title>How glucocorticoid suppress immunity</title></json:item><json:item><host><author></author><title>Munck, A. & P. M. Guyre. 1992. In Psychoneuroimmunology. R. Ader, D. L. Felten & N. Cohen, Eds. Vol. 2: 447‐474. Academic Press. San Diego.</title></host></json:item><json:item><author><json:item><name>A. Munck</name></json:item></author><host><volume>5</volume><pages><last>44</last><first>25</first></pages><author></author><title>Endocr. Rev.</title></host><title>Physiological functions of glucocorticoids in stress and their pharmacological actions</title></json:item><json:item><author><json:item><name>G. P. Chrousos</name></json:item></author><host><volume>332</volume><pages><last>1362</last><first>1351</first></pages><author></author><title>N. Engl. J. Med.</title></host><title>The hypothalamus‐pituitary‐adrenal axis and immune‐mediated inflammation</title></json:item><json:item><author><json:item><name>E. M. Sternberg</name></json:item></author><host><volume>86</volume><pages><last>2378</last><first>2374</first></pages><author></author><title>Proc. Natl. Acad. Sci. USA</title></host><title>Inflammatory mediator‐induced hypothalamic‐pituitary‐adrenal axis activation is defective in streptococcal cell wall arthritis‐susceptible Lewis rats</title></json:item><json:item><author><json:item><name>A. E. Calogero</name></json:item></author><host><volume>55</volume><pages><last>608</last><first>600</first></pages><author></author><title>Neuroendocrinology</title></host><title>Neurotransmitter‐induced hypothalamic‐pituitary‐adrenal axis responsiveness is defective in inflammatory disease‐susceptible Lewis rats: In vivo and in vitro studies suggesting globally defective hypothalamic secretion of corticotropin‐releasing hormone</title></json:item><json:item><author><json:item><name>E. M. Sternberg</name></json:item></author><host><volume>86</volume><pages><last>4775</last><first>4771</first></pages><author></author><title>Proc. Natl. Acad. Sci. USA</title></host><title>A central nervous system defect in biosynthesis of corticotropin‐releasing hormone is associated with susceptibility to streptococcal cell wall‐induced arthritis in Lewis rats</title></json:item><json:item><author><json:item><name>E. M. Sternberg</name></json:item></author><host><volume>570</volume><pages><last>60</last><first>54</first></pages><author></author><title>Brain Res.</title></host><title>Corticotropin releasing hormone related behavioral and neuroendocrine response to stress in Lewis and Fisher rats</title></json:item><json:item><author><json:item><name>K. Schauenstein</name></json:item></author><host><volume>139</volume><pages><last>1833</last><first>1830</first></pages><author></author><title>J. Immunol.</title></host><title>Disturbed immuno‐endocrine communication in autoimmune disease. Lack of corticosterone response to immune signals in obese strain chickens with spontaneous autoimmune disease</title></json:item><json:item><author><json:item><name>G. Wick</name></json:item></author><host><volume>29</volume><pages><last>142</last><first>136</first></pages><author></author><title>Isr. J. Med. Sci.</title></host><title>Altered neuroendocrine communication in autoimune disease</title></json:item><json:item><author><json:item><name>G. Wick</name></json:item></author><host><volume>14</volume><pages><last>563</last><first>539</first></pages><author></author><title>Endocr. Rev.</title></host><title>Immunoendocrine communication via the hypothalamo‐pituitary‐adrenal axis in autoimmune diesease</title></json:item><json:item><author><json:item><name>J. M. Cash</name></json:item></author><host><volume>19</volume><pages><last>1696</last><first>1692</first></pages><author></author><title>J. Rheumatol.</title></host><title>Pituitary‐adrenal axis responsiveness to ovine CRH in patients with rheumatoid arthritis treated with low‐dose prednisolone</title></json:item><json:item><author><json:item><name>R. Schlaghecke</name></json:item></author><host><volume>35</volume><pages><last>746</last><first>740</first></pages><author></author><title>Arthritis Rheum.</title></host><title>Glucocorticoid receptors in rheumatoid arthritis</title></json:item><json:item><author><json:item><name>A. T. Reder</name></json:item></author><host><volume>12</volume><pages><last>198</last><first>195</first></pages><author></author><title>Interferon Res.</title></host><title>Interferon‐b treatment does not elevate cortisol in multiple sclerosis. 1992.</title></json:item><json:item><author><json:item><name>A. Buske‐Kirschbaum</name></json:item></author><host><volume>59</volume><pages><last>426</last><first>419</first></pages><author></author><title>Psychosom. Med.</title></host><title>Attenuated free cortisol response to psychosocial stress in children with atopic dermatitis</title></json:item><json:item><host><author></author><title>Buske‐Kirschbaum, A., K. von Auer, S. Jobst, W. Rauh, S. Weis & D. H. Hellhammer. 1997. Allergic asthma and stress reactivity in children: Further evidence for hyporesponsive hypothalamus‐pituitary‐adrenal (HPA) axis in atopic patients. Manuscript in preparation.</title></host></json:item><json:item><author><json:item><name>B. Heubeck</name></json:item></author><host><volume>39</volume><pages><last>17</last><first>12</first></pages><author></author><title>Hautarzt</title></host><title>Sind Verschiebungen des zirkadianen Cortisolrhythmus ein endokrines Symptom des endogenen Ekzems?</title></json:item><json:item><author><json:item><name>N. Buhles</name></json:item></author><host><volume>62</volume><pages><last>1363</last><first>1356</first></pages><author></author><title>Z. Hautk.</title></host><title>Disorders of steroid metabolism in inflammatory dermatoses</title></json:item><json:item><author><json:item><name>M. Rupprecht</name></json:item></author><host><volume>20</volume><pages><last>551</last><first>543</first></pages><author></author><title>Psychoneuroendocrinology</title></host><title>Cortisol, corticotropin, and b‐endorphin response to corticotropin‐releasing hormone in patients with atopic eczema</title></json:item><json:item><author><json:item><name>M. Rupprecht</name></json:item></author><host><volume>183</volume><pages><last>105</last><first>100</first></pages><author></author><title>Dermatologica</title></host><title>Elevated glucocorticoid receptor concentration before and after glucocorticoid therapy in periphera mononuclear leukocytes of patients with atopic dermatitis</title></json:item><json:item><author><json:item><name>L. Laue</name></json:item></author><host><volume>71</volume><pages><last>1480</last><first>1474</first></pages><author></author><title>J. Clin. Endocrinol. Metabol.</title></host><title>Effect of chronic treatment with the glucocorticoid antagonist RU 486 in man: Toxicity, immunological and hormonal aspects</title></json:item><json:item><host><author></author><title>Schultz Larsen, F. 1992. Genetic aspects of atopic eczema. In Handbook of Atopic Eczema. T. Ruzicka, J. Ring & B. Przybilla, Eds. Vol. 1: 9‐14. Springer Verlag. Berlin.</title></host></json:item><json:item><author><json:item><name>C. Kirschbaum</name></json:item></author><host><volume>75</volume><pages><last>1530</last><first>1526</first></pages><author></author><title>J. Clin. Endocrinol. Metabol.</title></host><title>Heritability of cortisol response to human corticotropin‐releasing hormone, ergometry, and psychosocial stress in humans</title></json:item><json:item><host><author></author><title>Besedovsky, H. & A. del Rey. 1992. Physiological implications of the immune‐neuro‐endocrine network. In Psychoneuroimmunology. R. Ader, D. L. Felten & N. Cohen, Eds. Vol. 2: 589‐608. Academic Press. San Diego.</title></host></json:item><json:item><author><json:item><name>R. M. King</name></json:item></author><host><volume>35</volume><pages><last>706</last><first>697</first></pages><author></author><title>Psychosom. Med.</title></host><title>Use of a diary technique to investigate psychosomatic relations in atopic patients</title></json:item><json:item><author><json:item><name>L. Melin</name></json:item></author><host><volume>115</volume><pages><last>474</last><first>467</first></pages><author></author><title>British J. Dermatol.</title></host><title>Behavioral treatment of scratching in patients with atopic dermatitis</title></json:item><json:item><author><json:item><name>D. H. Hellhammer</name></json:item></author><host><volume>60</volume><pages><last>17</last><first>8</first></pages><author></author><title>Psychother. Psychosom.</title></host><title>Endocrine correlates of stress vulnerability</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>840</volume><publisherId><json:string>NYAS</json:string></publisherId><pages><total>8</total><last>754</last><first>747</first></pages><issn><json:string>0077-8923</json:string></issn><issue>1</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1749-6632</json:string></eissn><title>Annals of the New York Academy of Sciences</title><doi><json:string>10.1111/(ISSN)1749-6632</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>multidisciplinary sciences</json:string></wos><scienceMetrix><json:string>general</json:string><json:string>general science & technology</json:string><json:string>general science & technology</json:string></scienceMetrix></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1111/j.1749-6632.1998.tb09613.x</json:string></doi><id>8F433D0008258B11E0B66804EDBBB8DC8A64220B</id><score>1.4104552</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/8F433D0008258B11E0B66804EDBBB8DC8A64220B/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/8F433D0008258B11E0B66804EDBBB8DC8A64220B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8F433D0008258B11E0B66804EDBBB8DC8A64220B/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1998</date></publicationStmt><notesStmt><note type="content">*This work was supported by the Deutsche Forshungsgemeinschaft (DFG), Grant HE 1013/13‐1.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title><author xml:id="author-1"><persName><forename type="first">A.</forename><surname>BUSKE‐KIRSCHBAUM</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">S.</forename><surname>JOBST</surname></persName><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">D. H.</forename><surname>HELLHAMMER</surname></persName><email>hellhamm@pcmail.uni‐trier.de</email><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation></author></analytic><monogr><title level="j">Annals of the New York Academy of Sciences</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="DOI">10.1111/(ISSN)1749-6632</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-05"></date><biblScope unit="volume">840</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="747">747</biblScope><biblScope unit="page" to="754">754</biblScope></imprint></monogr><idno type="istex">8F433D0008258B11E0B66804EDBBB8DC8A64220B</idno><idno type="DOI">10.1111/j.1749-6632.1998.tb09613.x</idno><idno type="ArticleID">NYAS747</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.</p></abstract></profileDesc><revisionDesc><change when="1998-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/8F433D0008258B11E0B66804EDBBB8DC8A64220B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="05001"><doi origin="wiley">10.1111/nyas.1998.840.issue-1</doi><titleGroup><title type="main">NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES</title></titleGroup><numberingGroup><numbering type="journalVolume" number="840">840</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="1998-05">May 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="72" status="forIssue"><doi origin="wiley">10.1111/j.1749-6632.1998.tb09613.x</doi><idGroup><id type="unit" value="NYAS747"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Neuroimmunomodulation: Molecular Aspects, Integrative Systems, and Clinical Advances<sup>a</sup>: Part III. Disturbances in Neuroendocrine‐Immune Interactions: Clinical, Behavioral, and Therapeutic Implications: Stress, Neuroendocrine Responses, and Allergic Disease</title></titleGroup><eventGroup><event type="firstOnline" date="2006-02-07"></event><event type="publishedOnlineFinalForm" date="2006-02-07"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-04-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="747">747</numbering><numbering type="pageLast" number="754">754</numbering></numberingGroup><correspondenceTo> Address for correspondence: D. H. Hellhammer, Center for Psychobiology and Psychosomatic Research, University of Trier, D‐54286 Trier, Germany; Telephone: 49‐651‐2012929; Fax: 49‐651‐2012934; e‐mail: <email normalForm="hellhamm@pcmail.uni-trier.de">hellhamm@pcmail.uni‐trier.de</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS747.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="37"></count><count type="linksCrossRef" number="33"></count></countGroup><titleGroup><title type="main">Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?<link href="#fn1"><sup>a</sup></link></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>A.</givenNames><familyName>BUSKE‐KIRSCHBAUM</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>JOBST</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" corresponding="yes"><personName><givenNames>D. H.</givenNames><familyName>HELLHAMMER</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>A<sc>bstract</sc>: </b> Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label>a</label><p>This work was supported by the Deutsche Forshungsgemeinschaft (DFG), Grant HE 1013/13‐1.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?a</title></titleInfo><name type="personal"><namePart type="given">A.</namePart><namePart type="family">BUSKE‐KIRSCHBAUM</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">JOBST</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. H.</namePart><namePart type="family">HELLHAMMER</namePart><affiliation>Center of Psychobiology and Psychosomatic Research, University of Trier, D54286 Trier, Germany</affiliation><affiliation>E-mail: hellhamm@pcmail.uni‐trier.de</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1998-05</dateIssued><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="references">37</extent></physicalDescription><abstract>Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin‐E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus‐pituitary‐adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune‐related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.</abstract><note type="content">*This work was supported by the Deutsche Forshungsgemeinschaft (DFG), Grant HE 1013/13‐1.</note><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>1998</date><detail type="title"><title>NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES</title></detail><detail type="volume"><caption>vol.</caption><number>840</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>747</start><end>754</end><total>8</total></extent></part></relatedItem><identifier type="istex">8F433D0008258B11E0B66804EDBBB8DC8A64220B</identifier><identifier type="DOI">10.1111/j.1749-6632.1998.tb09613.x</identifier><identifier type="ArticleID">NYAS747</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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